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Neuro Rehab 1 > Neuroplasticity and Neuro Rehab > Flashcards

Neuroplasticity and Neuro Rehab Flashcards

1
Q

what are ways the CNS can be damaged (7)

A

trauma
metabolic disturbances
toxicity
infection
ischemia and infarction
hemorrhage
dz

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2
Q

what is the cellular cascade initiated by CNS lesions

A
  1. K+ exits; Na, Cl, Ca enter
  2. H2O follows Na into cells = edema
  3. glutamate & aspartate released
  4. enzyme disturbances follow & free radicals, lipases released
  5. cell membranes, genetic material in cells are damaged and die w/i 5-10min if O2 & glucose supply not restored
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3
Q

what are glutamate and aspartate and what is their role

A

cytotoxic
causes additional cell death

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4
Q

how does a TIA fit in w cascade of cellular changes seen after CNS lesions

A

TIA = stoppage of flow, had deficits and then flow resumed
- stoppage so long that level of cell death was accelerated

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5
Q

how does CNS “shock” present in the acute stages (5)

A

altered LOC
hypotonia
motor and sensory changes
cognitive deficits
decline in function

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6
Q

what is the pathophys behind CNS “shock” in acute stages

A

absence or slowing of neuron firing

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7
Q

what is the ischemic zone or core of a CNS lesion

A

directly damaged

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8
Q

what is the penumbra of a CNS lesion

A

area adjacent to ischemic core
- outer rim

can be damaged also
dec activity and availability of certain enzymes

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9
Q

what is the diaschisis

A

reduced activity in other parts of the CNS d/t loss of connectivity and communication w lesioned area(s)

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10
Q

what is the time line of the existence of CNS shock

A

lasts 5ish days
- get tone afterward

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11
Q

what is the goal of medical management when recovering from a CNS lesion

A

restore blood flow to ischemic core and penumbra as quickly as possible

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12
Q

how is blood flow restored to tissue in the penumbra and what is the significance of this

A

collateral circulation

collateral flow can only meet energy demands for several hours

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13
Q

what are 2 important considerations when medically managing a CNS lesion

A

edema has to be managed
ICP regulated

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14
Q

how can the ICP be regulated

A

meds (TPA)
craniectomy

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15
Q

what specifically allows for the recovery of CNS lesions

A

neuroplasticity

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16
Q

why can recovery occur spontaneously

A

edema subsides
metabolic pathways restored

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17
Q

what does the evidence show for PT when recovering from CNS lesions

A

PT can inc rate and degree of recovery and neuroplastic changes
- want to be aggressive in acute/intense phase

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18
Q

neuroplasticity

A

ability of nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function, and neuronal connections

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19
Q

what are two processes that allow for neuroplasticity in the presence of CNS lesions

A
  1. neural connections vary in response to environment/stimuli, activity, demands, cellular environment
  2. cellular mechanism for brain to encode learning and recover from lesions
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20
Q

what should be avoided while healing

A

sugars/salts - dec metabolic healing
stressful environments

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21
Q

when is neuroplasticity greatest

A

greatest rate in fetal stage to 2yo
- capability declines w aging but still possible

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22
Q

would there be lasting deficits from a childhood trauma

A

prob not functionally
may present cognitively

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23
Q

what are methods of imaging for assessing neuroplasticity

A

fMRI
SPECT
PET

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24
Q

what is neurogenesis

A

formation of new neurons throughout lifespan

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25
Q

how does neurogenesis change w age

A

fairly limited in adult mammals

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26
Q

where is neurogenesis more prominent

A

dentate gyrus of hippocampus

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27
Q

what happens in the hippocampus

A

learning and memory process

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28
Q

what is synaptic uncovering

A

chemically induced activity in previously inactive synapses

recruitment of formerly “silent” synapses

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29
Q

what is synaptogenesis

A

formation of new synaptic connections via axonal sprouting

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30
Q

reactive vs regenerative synaptogenesis

A

reactive - from nearby, healthy axons
regenerative - damaged axon

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31
Q

what is the goal of cortical remapping

A

functional substitution

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32
Q

what is cortical remapping

A

intact regions of the cortex assume the function of damaged areas

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33
Q

how can cortical remapping be assessed on imaging

A

fMRI
- what part of the brain lights up to complete a task (how was it restructured)

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34
Q

what are 4 mechanisms of neuroplasticity

A

neurogenesis
synaptic uncovering
synaptogenesis
cortical remapping

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35
Q

what is BDNF

A

brain derived neurotrophic factor

highly abundant neurotrophin in mammal brains

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36
Q

what is BDNF a key protein for

A

neuroplasticity processes
- helps to aid in neuroplasticity

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37
Q

what can impact BDNF levels and activity

A

physical activity inc levels

genetic polymorphisms affect BDNF activity and neuroplastic potential

38
Q

spontaneous recovery mechanisms are limited to what? what is the impact of this?

A

10 wks after stroke
- inflammation reduced and metabolic pathways restored

this is where the 3hrs a day model is from
- high levels of intense and meaningful rehab

39
Q

how can plasticity be harmful

A

reliance on unaffected side associated w neuroplastic changes may limit engagement of impaired side and results in learned non-use

40
Q

what is neurorehabilitation

A

goal based motor training for recovery of impaired or lost motor function

41
Q

since healing happens whether we do anything or not, what do we want to do w our interventions

A

want restructuring to be helpful, not harmful
- ms properly aligned, good blood flow to cells in the area

42
Q

what is the goal of neurorehab when it comes to fostering recovery

A

foster recovery via neuroplasticity whenever possible

43
Q

what cases do you see better potential for neuro rehab in

A

focal, stable lesions
early stages of some progressive conditions

44
Q

recovery via neuroplasticity requires active participation in: (3)

A
  1. goal directed, challenging activities
  2. age appropriate and salient activities to inc motivation
  3. repetition is key
45
Q

what is difficult ab neuro rehab

A

no protocols exist and limited agreement
- makes prescription and dosing a challenge

ex: even the typical 3hrs might not be sufficient

46
Q

acute vs chronic phase of CNS lesion

A

acute - steep recovery curve in 3-6mo period
chronic - after 6mo

47
Q

how does the rate of recovery change in acute vs chronic stages

A

rate of recovery slows in chronic phase
- still possible

48
Q

if there has been a period of semi-automatic recovery, what does this mean for neuroplasticity

A

can still be induced after this period

49
Q

what are 6 additional considerations for neuroplasticity

A

age
nature of lesion
co-morbidities
PLOF
cognition, motivation, mood
genetic factors

50
Q

what does age mean for neuroplasticity

A

younger is better

51
Q

how can the nature of the lesion impact neuroplasticity

A

focal vs global
- focal is one point (better)
- global - everywhere, harder to nail down

stable vs progressive
- stable - TBI/stroke (better)
- progressive - evolving, ie MS

52
Q

what are comorbidities to consider for neuroplasticity? why are these relevant?

A

BMI
cardiac/respiratory hx

harder to push them for acute intense therapy

53
Q

what about PLOF should be considered for neuroplasticity

A

fitness
activity level
degree of interconnections established

54
Q

how can CNS lesion impact motivation

A

poor motivation
- where injury is can cause depression
- having brain injury itself can be hard to cope w

good motivation in unsafe context
- people might not realize have a brain injury

55
Q

why genetic factors should be considered for neuroplasticity

A

how are they going to heal
how well will they heal

56
Q

what are components/strategies of neurorehab that promote neuroplastic changes

A

applied motor learning principles
- practice schedules
- feedback
- environment

prevent learned non-use
- CIMT

use of tech
- VR, robotics
- motor imagery

57
Q

what role does environment paly in creating neuroplastic changes

A

more challenging vs easier environments
- d/t noise, dynamic, business

58
Q

what is CIMT

A

constraint induced movement therapy

forced used of involved limb
- uninvolved limb is constrained via sling, oven mit, etc. and involved limb engaged in challenging and meaningful tasks

59
Q

evidence for CIMT and recovery

A

strong

60
Q

who is CIMT appropriate for

A

people w weakness in involved and not complete paralysis

61
Q

what can BWSTT be combined w in training

A

VR or robotics

62
Q

what is BWSTT

A

body weight support treadmill training

allows PT to facilitate normal gait pattern safely, more steps per session, improved body mechanics but may require more staff

63
Q

research and BWSTT?

A

effective but no more so than overground training

64
Q

what can robotic neurorehab devices be used for specifically

A

training tool and mechanism

65
Q

evidence for robotic neurorehab devides

A

good evidence but costly and not widely available
- requires specialized training of PT

66
Q

what systems does VR tap into

A

emotional and motivational systems

67
Q

what is VR and how is it applied in therapy

A

virtual reality
immersive, 3D, computer-generated environment

interact w or manipulate objects in virtual setting, thereby creating a safe and controlled milieu for therapy sessions

68
Q

what population has VR been especially effective in?

A

peds

69
Q

how is VR effective for neurorehab

A

inc motivation and compliance which promotes neuroplasticity and recovery thru inc reps of activities

70
Q

why has there been an inc use of VR in neurorehab

A

recent dec in cost for systemes
emergence of commercially available serious games

71
Q

what is rTMS

A

repetitive transcranial magnetic stim

rTMS to motor cortex can inc excitability of affected hemisphere and inhibit unaffected hemisphere to promote balance and functional reorganization

72
Q

how does neuroplasticity change over stages of injury as evidenced by TMS mapping of corticospinal system

A

different neuroplastic mechanisms may occur at different stages

73
Q

how does rTMS work

A

magnet placed over area of damage or the opposite side (depending on communication)
- depression on active side
- active side no longer inhibiting actions on other side of brain
- other side of brain can continue inhibiting the active side and further depresses it

74
Q

where can FES be used

A

long term to compensate for motor loss, inc safety and independence
- ie lack of DF in gait

75
Q

literature and FES

A

varied findings for recovery

76
Q

what is required for motor imagery to work

A

intact cognition

77
Q

what is a pro of motor imagery

A

free
no special training

78
Q

what does motor imagery activate

A

same motor pathways as physical movement
similar physiological responses to overt movement

79
Q

why do you always want to do motor imagery

A

every time you think ab doing the action, the neuronal pathway is trying to push thru to the ms and do it
- eventually “plow thru snow pile” and will activate ms (hopefully)

80
Q

what is regen med and rehab

A

interprofessional field of research and clinical practice for repair, replacement or regen of cells, tissues, and/or organs in order to restore function lost due to dz or damage

81
Q

what has led to a rapid proliferation of research in regen med and rehab

A

recent advances in stem cell and tissue engineering tech

82
Q

what are limitations to regen med

A

survival and appropriate differentiation of implanted cells as well as limiting proliferation

83
Q

who is a good candidate for regen med and stem cell implantation

A

stable (not too much inflammation or bleeding)

correct genetic programming to convert available STEM cell into cell it needs to be
- don’t want to let it proliferate too much

84
Q

what is regen med looking for in pts

A

if there is additional STEM cells or nerves to regen

85
Q

regen med: studies show greater recovery in who

A

greater recovery w combination of stem cell plus rehab

rather than either approach used in isolation in animal model studies

86
Q

pt w too much inflammation and bleeding means what for rehab

A

focus on stabilizing them medically than PT rehab

87
Q

what instances in pts are you thinking that recovery isn’t possible

A

global deficits
dec level of arousal and awareness

advanced, progressive dz or neurodegenerative process

88
Q

if recovery isn’t possible, what does this mean for rehab

A

look for ways to compensate or substitute

89
Q

compensation vs substitution

A

compensation - use of AD, w/c, AFO to mobilize

substitution - can’t do motion you want, but use other ms to create different movement to reach the same goal

90
Q

what are examples of substitutions

A

tenodesis grasp (often in SCI)
- use automatic finger flex when extend wrist to pick something up

circumduction in swing phase of gait d/t loss of rectus fem

Neuro Rehab 1 (27 decks)

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